Growth hormone treatment for six months after weight loss surgery prevents loss of muscle mass

August 22, 2015

Weight loss surgery techniques, such as gastric banding, have been shown to be effective in reducing body weight and obesity-related diseases, such as diabetes. Although the results of these procedures are widely beneficial, there are some complications. Following surgery, patients are at risk of losing needed lean body mass and skeletal muscle mass due to the serious complications associated with rapid and sustained weight loss. This new study investigated whether growth hormone treatment could prevent or reduce these losses.

"Besides its more commonly known effect on linear growth during childhood, growth hormone benefits body composition throughout life by increasing muscle mass and reducing fat mass," said Dr. Silvia Savastano, M.D., Ph.D., researcher at University Federico II of Naples in Italy and lead author of the study. "The results of our study show that the use of short-term treatment with growth hormone during a standardized program of low calorie diet and physical exercise is effective in reducing the loss of muscle mass and increasing the loss of fat mass after bariatric surgery."

In this study, Dr. Savastano and her colleagues evaluated women who underwent laparoscopic-adjustable silicone gastric banding surgery and were diagnosed with growth hormone deficiency after the procedure. These women were divided into two groups where both groups participated in a standardized diet and exercise program, but only one group also received growth hormone. After a follow-up period of six months, women receiving growth hormone experienced a significant decrease of fat mass and an increase in lean body and skeletal muscle mass.

"This evidence opens a new frontier for growth hormone therapy in the management of morbidly obese patients," said Dr. Savastano. "However, growth hormone treatment can be costly and a careful cost-benefit analysis that also takes into account the cost of commonly used therapy for management of morbidly obese patients is needed."


They've now found that the inflammatory factor CXCL10 (also known as Interferon-gamma-inducible Protein-10, or IP-10) is an important trigger for beta cells' destruction. They found that hormone-producing cells isolated from patients with type 2 diabetes secrete CXCL10 and contain more than 30 times the amount of the CXCL10 message in the form of RNA than do cells from patients without diabetes.

Pancreatic sections taken from obese people without diabetes as well as those with type 1 or type 2 diabetes showed CXCL10 in the beta cells, they found. Moreover, treatment of isolated human pancreatic cells with CXCL10 decreased beta cell viability and impaired the production and secretion of insulin. They traced those effects of CXCL10 to a well-known pathway of the innate immune system involving a protein known as toll-like receptor 4 (TLR4).

The new data suggest a potential mechanism for the switch from beta cells' proliferation to their programmed cell death, the researchers concluded. "To prevent such a progression using anti-inflammatory targets of the TLR4 signaling pathway will be of high importance to rescue the beta cell from inflammation-induced self-destruction and [to] preserve beta cell function and mass."